J Clin Gastroenterol ​2003;37(2):119–124. © 2003 Lippincott Williams & Wilkins, Inc.

​ herapeutic Recommendations
Clinical Reviews T
Corrosive Ingestion in Adults
Kovil Ramasamy, MD, and Vivek V. Gumaste, MD, MRCP(I), FACG
Abstract ​Ingestion of a corrosive substance can produce severe injury to the gastrointestinal tract and can even result in death.
The degree and extent of damage depends on several factors like the type of sub- stance, the morphologic form of the agent, the
quantity, and the intent. In the acute stage, perforation and necrosis may occur. Long-term complications include stricture
formation in the esophagus, antral stenosis and the development of esophageal carcinoma. Endoscopy should be attempted and
can be safely per- formed in most cases to assess the extent of damage. Procedure- related perforation is rare. Stricture formation
is more common in patients with second and third degree burns. Corticosteroids may help prevent stricture formation. Esophageal
carcinoma may de- velop beginning 30 to 40 years after the time of injury. ​Key Words: ​lye ingestion, corrosives, sodium
hydroxide

A​ ccording ​
ciation of ​
to ​
Poison ​
the annual ​
Control, ​
report ​
there ​
of ​
were ​
the ​
206,636 ​
American ​
cases ​
Asso- ​
of

human exposure to cleaning substances (which include ac- ids and alkalis) in 2000. Twenty-seven of these cases (the
majority being instances of ingestion) resulted in death.​1 ​Although children account for 80% of accidental ingestion,​2
ingestion in adults is more often suicidal in intent and there- fore tends to be more serious. Corrosive agents produce
extensive damage to the gastrointestinal tract, which may result in perforation and death in the acute phase. Long
term complications include stricture formation and the develop- ment of esophageal carcinoma.
SUBSTANCES ​Corrosives can be alkaline in nature or acids. Lye is a general term used for alkali found in cleaning
agents.
Alkalis
Alkaline material accounts for most cases of caustic in- gestion in western countries.​2 ​Alkalis can be found in a
variety of cleaning agents, drain openers, bleaches, toilet bowl cleaners, and detergents (Table 1).
119
Most commonly used household bleaches contain hydro- gen peroxide (3%), sodium hypochlorite or low concentra-
tions of sodium hydroxide (1%), and are mild to moderate irritants with a pH ranging from 10.8 to 11.4.​3 ​Accidental
ingestion produces minimal injury to the gastrointestinal tract; long-term damage including stricture formation is
rare. However, the ingestion of large quantities of bleach may be associated with serious damage.
Unlike bleaches, drain cleaners are more dangerous. Drain cleaners contain sodium hydroxide in concentrations
ranging from 4% to 54% and the crystalline variety tends to contain a higher concentration of sodium hydroxide than
the liquid form. These agents can produce severe harm to the gastrointestinal tract including perforation. Stricture
forma- tion is consistently seen with ingestion of drain cleaners.
Automatic dishwasher detergents contain sodium phos- phate or tripolyphosphate that are also powerful corrosive
agents.​1 ​Clinitest and denture cleaning tablets contain so- dium hydroxide and these can cause major esophageal in-
juries because their solid form prolongs the duration of contact with the mucosa.​4
Hair relaxer, a commercially available alkaline product, is another agent implicated in caustic ingestion. Although
these products produce extensive facial injury and oral burns, significant esophageal damage has not been reported.​5

Acids​Acid ingestion tends to occur less frequently in the United

​ States (<5%) but appears to be more common in
countries like India where hydrochloric acid and sulfuric acid are easily accessible.​6 ​In the United States, acids are
generally available as toilet bowel cleaners (sulfuric, hydro- chloric), anti rust compounds (hydrochloric, oxalic,
hydro- fluoric), battery fluids (sulfuric), and swimming pool cleaners (hydrochloric).
PATHOPHYSIOLOGY ​Solutions with a pH of less than 2 or greater then 12 are
From The Department of Medicine, Mount Sinai Services, City Hos- pital Center at Elmhurst, New York and the Mount Sinai School of Medi-
 highly corrosive. Alkali produces liquefaction necrosis.​2 ​A 22.5% solution of NaOH in contact with the esophagus
for ​cine of the City University of New York, New York.
Address correspondence and reprint requests to Dr. Vivek V. Gumaste, Division of Gastroenterology, Mount Sinai Services at Elmhurst, 79-01
Broadway, Elmhurst, New York, NY 11373, USA.
10 seconds and 30% NaOH for 1 second can produce a full thickness injury.​2 ​Thrombosis of small vessels and
produc- tion of heat exacerbate the initial corrosive injury. Tissue
formation and this may limit tissue penetration, but this
does not ap- pear to be a major variable in determining the
extent of injury. Although some earlier studies​10,11 ​indicated
that acid preferentially damages the stomach, recent
studies​6 ​have reported extensive damage to the esophagus
as well.
The pathologic classification of caustic injury to the
esophagus is similar to classification of burns to the skin
and is elaborated in Table 2. The degree of injury correlates
directly with stricture formation and mortality. Over 80%
of patients with grade 3 burns go on to stricture formation
while one-third of those with grade 2 burns may stenose.​7
Stricture formation is extremely rare in injuries of the first
degree. Mortality is also more common in grade 3 injury.​7

CLINICAL PRESENTATION ​The clinical

injury progresses rapidly in the first few minutes but can presentation depends upon the type of the substance,
continue for several hours. Mucosal sloughing occurs 4 to 7 amount, and physical form of the substances. Solid alkali
days after the initial injury, and bacterial invasion, inflam- adheres to the mouth and pharynx producing maximum
matory response, and development of granulation tissue en- damage to these areas while relatively sparing the
sue. Because collagen deposition may not begin until the esophagus. In contrast the liquid form transits rapidly
second week, the tensile strength of the healing tissue is through the mouth and pharynx and produces its greatest
low during the first 3 weeks. Many people therefore caustic effect on the esophagus.​2
advocate avoiding endoscopy between 5 to15 days after
Hoarseness and stridor may be seen suggesting
caustic in- gestion.​7 ​Scar retraction begins by the third week
laryngeal or epiglottic involvement. Symptoms of
and may continue for several months. This results in
esophageal in- volvement include dysphagia and
stricture forma- tion and shortening of the involved
odynophagia, whereas epigastric pain and hematemesis
segment of the gastro- intestinal tract. Shortening of the
may be manifestations of stomach involvement. However,
esophagus alters the LES pressure leading to increased
the absence of pain does not preclude significant
gastroesophageal reflux, which in turn accelerates stricture
gastrointestinal damage. Sometimes massive hematemesis
formation.​8 ​Esophageal injury due to caustic ingestion also
can occur as a result of an aortoen- teric fistula.​2
produces changes in esophageal motility resulting in low
Perforation of the stomach or the esophagus can occur
amplitude and non- peristaltic contractions.​9
at any time during the first 2 weeks.​2 ​Hence, any change in
The degree of injury produced depends, to some
the clinical condition of the patient such as worsening of
extent, on the physical form of the alkali. Crystals or solid
ab- dominal pain or the appearance of chest pain should be
particles adhere to the mucous membrane making it
promptly investigated by radiologic studies
difficult to swal- low and thereby diminishing the injury
Studies have tried to ascertain whether the presenting
produced to the esophagus. On the other hand, liquid alkali
signs and symptoms accurately predict esophageal injury.
is easily swal- lowed, being tasteless and odorless, and is
While one study​12 ​claimed that stridor was 100% specific
most likely to damage the esophagus and stomach.​2
for significant esophageal injury another study​13 ​indicated
Acid induces coagulation necrosis with eschar
that no single symptom or group of symptoms could accu-
rately predict esophageal injury. Asymptomatic children
with unintentional caustic ingestion usually do not have
significant lesions on endoscopy.​14
Ten to 30 percent of patients with esophageal burns
J Clin Gastroenterol, Vol 37, No. 2, 2003 ​120
have no oropharyngeal damage.​2 ​One study reported
esophageal injury in 37.5% of patients without oral damage
and twenty- two percent of these were grade 2 or 3
lesions.​15 ​Upto​16

TABLE 1. ​Common household corrosives

Product Contents

Chlorox Sodium hypochlorite (5.25%) Peroxide Hydrogen Peroxide (3%) Tilex mildew
remover Sodium hypochlorite (5%), sodium hydroxide (1%) Electrasol dishwasher
detergent Sodium tripolyphosphates (20%–40%) Cascade dishwater detergent
Phosphates (25%–50%) Comet cleanser Trisodium phosphate (14.5%) Polident powder
Sodium tripolyphosphate (<15%) Drano (liquid) Sodium hydroxide (9.5%) Drano
Professional (liquid) Sodium hydroxide (32%) Crystal Drano (granular) Sodium
hydroxide (54%) Liquid Plummer Sodium hydroxide (0.5%–2%)
Sodium hypochlorite (5%–10%) Dow oven cleaner
Sodium hydroxide (4%) Mister Plumber Sulfuric acid (99.5%) Lysol
toilet cleaner Hydrochloric acid (8.5%)
complication of acid ingestion, it can also occur with lye
injury to the stomach.​18 ​3. Esophageal carcinoma is a
well-known sequel of lye ingestion.​2 ​The latent period
between the time of inges- tion and the development of
carcinoma may be as long as 58 years. There is a 1000- to
3000-fold increase in the incidence of esophageal
carcinoma after lye ingestion, and up to 3% of patients with
carcinoma of the esopha- gus may have history of caustic
ingestion. Most lesions occur at the level of the carina.
70% of patients with oropharyngeal burns do not have sig-
Patients with carcinoma of the esophagus due to lye
nificant damage to the esophagus. Injuries of the orophar-
ingestion may have a better prognosis than other patients,
ynx are therefore not a reliable index of damage to
as they tend to be younger and tend to have earlier
esophagus.
symptoms.​2 ​4. Gastric carcinoma is a rare occurrence in
No one sign or group of signs was 100% accurate in
patients with a
predicting positive or negative endoscopies. ​Late Sequelae
history of caustic injury.​2
1. Stricture formation may become symptomatic within 3
months or may even manifest a year later.​2 ​Ingestion of MANAGEM
liquid lye is most likely to induce stricture formation than ENT Pre Hospital Measures
solid crystals. Lye induced strictures tend to be long (Fig. Gastric lavage and induced emesis are
1).​2 ​Indwelling nasogastric tube may also contrib- ute to the contraindicated because re-exposure of the esophagus to
increased formation of long strictures. 2. Gastric outlet the corrosive agent tends to produce additional injury. Milk
obstruction: Symptoms of early satiety and weight loss may and water have been used as antidotes but their
suggest gastric outlet obstruction. This tends to occur less effectiveness has not been proven. Furthermore heat
frequently than stricture formation, being noted in only 4 of generated by the chemical reac- tion may increase the
214 patients in 1 study.​17 ​This complication may be seen damage. Milk may also obscure
within 5 or 6 weeks or may present for the first time after subsequent endoscopy. Activated charcoal is also contrain-
dicated for the same reason. ​Radiologic Studies
several years.​2 ​Although initially thought to be a specific
 In the acute phase, a plain chest radiograph may in a patient with history of lye ingestion.
reveal air in the mediastinum suggesting esophageal
perforation. Likewise free air under the diaphragm may
indicate gastric perforation. If it is necessary to confirm
perforation, the classic teaching is that a water-soluble
agent like hypaque or gastrograffin should be used as they
are less of an irritant to the mediastinum and peritoneal
cavity compared with barium sulfate. However, some
investigators feel that both

FIGURE 1. ​UGI series showing a long esophageal stricture

Ramasamy and Gumaste Corrosive Ingestion in Adults ​121

TABLE 2. ​Endoscopic grading of corrosive esophageal injury

Grade 0 Normal findings on endoscopy Grade 1 Edema, hyperemia of mucosa Grade 2a

Friability, blisters, hemorrhages, erosions, whitish membranes, exudates and
superficial ulceration’s Grade 2b Grade 2a plus deep discrete or circumferential ulcerations
Grade 3a Small scattered areas of multiple ulcerations and areas of necrosis
(brown-black or grayish discoloration) Grade 3b Extensive
necrosis
are equally irritants.​19 ​Endoscopy is the diagnostic proce-
dure of choice in the absence of perforation.
Barium studies may be helpful as a follow-up
measure and for the evaluation of complications. In fact,
barium sulfate is the preferred contrast agent for an
anatomically intact but scarred gastrointestinal tract. It is
radio opaque, provides greater radiographic details than
water-soluble contrast agents, and is relatively nonirritant
to the pulmo- nary tissues in case it is aspirated into the
lungs.
Endoscopy (Table 3)
The oropharynx needs to be first examined by
laryngos- copy. A supraglottic or epiglottic burn with
erythema and edema formation may be a harbinger of
airway obstruction and should be seen as an indication for
early endotracheal intubation or tracheostomy. A third
degree burn of the hy- popharynx is a contraindication for
endoscopy.
Indication
s managed appropriately.
There are no strict guidelines as to who needs
endoscopy and who does not. However the following
factors may be taken into account when making the
decision.
(a) Substance. Household bleach ingestion in asymptomat-
ic children does not warrant endoscopy.​20 ​Similarly en-
doscopy may not be necessary in asymptomatic children
who have ingested hair relaxer.​21 ​(b) Quantity. Ingestion of
larger quantities of corrosives is usually associated with
greater damage. Although it is difficult to exactly quantify
the amount, a cupful may be associated with significant
injury while a teaspoonful may not. (c) Intention. Serious
damage is noted when the intent is suicidal and endoscopy
is usually indicated in such circumstances. (d) Symptoms.
Persistent symptoms also warrant endo-
scopic examination.
Timin
g always imply extension of the same degree of injury to
Some previous studies have tried to stipulate the
timing of endoscopy indicating when it should be done and
when it should not be done. Endoscopy can be performed
preferably within 12 hours and generally not later than 24
hours al-
TABLE 3. ​Endoscopic management
1. Initial endoscopy should be performed as soon as possible as
long as the patient is stable and there is no evidence of
perforation. 2. Third degree burns of the hypopharnyx is a
contraindication to
endoscopy. 3. A complete but careful examination of the
esophagus and
though some authors state that endoscopy can be safely
performed up to 96 hours post-ingestion.​7 ​Wound softening
begins after 2 to 3 days and lasts up to 2 weeks making
endoscopy risky during this period. Endoscopy is usually
avoided from 5 to 15 days after corrosive intake.​7
Endoscopy should be performed as soon as possible
be- cause it serves a dual purpose. First, patients with no
evi- dence of gastrointestinal injury can be discharged,
provided there are no other complications. In fact, more
than 50% of patients, with history of caustic ingestion, have
no evi- dence of injury to the gastrointestinal tract.​2
Secondly, pa- tients with evidence of severe injury can be
Risk of Perforation
Early reports advocated general anesthesia and
endotra- cheal intubation prior to upper endoscopy because
of the risk of perforation . However it was discovered that
perfo- rations were more likely to occur when rigid
instruments were used and in children or uncooperative
patients. The use of flexible endoscopy has made this
procedure, in this situ- ation, safer. No procedure related
perforation occurred in series of 381 examinations reported
in one study.​7 ​Other authorities also concur with this
finding.​22 ​However the need for adequate sedation is
emphasized. Endotracheal in- tubation is required only for
patients in respiratory distress.
Extent
Every attempt must be made to assess the esophagus,
stomach, and duodenum provided it can be done safely.
Presence or absence of burns in the esophagus does not
stomach. Therefore it is important to examine the stomach
and the first part of duodenum, as well, in every patient.
Generally accepted recommendations are that the
endo- scope should be advanced until a circumferential
second- degree burn or third degree burn is seen.​4 ​Attempts
to continue past this point may increase the risk of
mechanical perforation. Endoscopic findings may be
graded as shown in Table 2.
In cases where endoscopy is terminated at the point of
esophageal or gastric injury, the duodenum must then be
evaluated by barium studies. Since severe duodenal injuries
can involve the neighboring structures, double contrast CT
J Clin Gastroenterol, Vol 37, No. 2, 2003 ​122
scan should be performed in stable patients with endoscopic
or radiologic evidence of significant duodenal abnormality
to inspect those areas of gastrointestinal tract such as the
colon, pancreas, and small bowel that are not routinely
evaluated after caustic ingestion.​23

stomach must be attempted. 4. Endoscope can be safely
advanced until a circumferential
burn is seen. 5. Prudent to avoid endoscopy between days
5–15 as tissue
softening increases the danger of
perforation. 6. Risk of procedure related
perforation is low.
Oral Intake
Patient whose injuries are graded 1 and 2a are
permitted oral intake and discharged within days with
antacid therapy. In more severe cases of damage (grades 2
or 3), observation in an intensive care unit and nutritional
support is required.
Prevention of Strictures
Stricture formation is the most important
complication of corrosive damage to the esophagus.
Attempts to prevent stricture formation include steroid use,
stenting, use of in- dwelling nasogastric tube, and early
dilatation.
Steroid
s
Although animal studies had shown that the use of
ste- roids after alkali injury decreases the incidence of
stricture formation, studies in humans have been
inconclusive so far.​2 ​A prospective study​24 ​conducted in 60
children over an 18 year period concluded that there was no
benefit from the use of corticosteroids. This study was
severely limited by its small numbers. The results of a meta
analysis​25 ​in 361 sub- jects from a total of 13 studies
produced more encouraging results. Strictures occurred in
40% of patients not receiving corticosteroids and
antibiotics compared with 19% in the treated group. The
difference was statistically significant.
The usual recommended dose of steroids is methyl
pred- nisolone 40 to 60 mg/ day intravenously. Steroids are
usu- ally given for at least 3 weeks.​2 ​Most investigators
would agree that since first degree burns of the esophagus
rarely if ever cause strictures, corticosteroids are not
necessary. It may be indicated in patients with third degree
burns, which invariably cause strictures. However the use
of corticoste- roids continues to be a debatable issue.
Antibiotic
s
With regard to the use of antibiotics, the data is not
very clear. Although in animals, antibiotics have shown to
de- crease infection in steroid treated esophageal burns, no
con- trolled trials in humans are available.​2 ​The consensus
however appears to be that patients treated with steroids
should be treated with antibiotics as well. A prophylac- tic
antibiotic, in the absence of steroid therapy, is not
advocated.​26
Nasogastric Tube
The insertion of nasogastric tube early in the course
of the treatment has been suggested to ensure patency of
the esophageal lumen​2 ​but one needs to be cautious because
a nasogastric tube itself can contribute to the development
of long strictures and routine use is not warranted.
Total Parenteral Nutrition
Some investigators are of the opinion that total
parental nutrition may prevent stricture formation, but the
available data is not very convincing.​2
Intraluminal Stent
The insertion of specially designed silicone rubber
stents may be helpful in preventing stricture formation after
caus- tic ingestion according to some studies.​27,28
Early Dilatation
Early dilatation starting after injury results in a high
in- cidence of perforation, and is not currently
recommended.​2
Sucralfate
Anecdotal reports suggest that the use of sucralfate
may decrease stricture formation.​29 ​Gastroesophageal
Reflux
Gastroesophageal reflux has a tendency to worsen the
caustic insult to the esophagus probably accelerating stric-
ture formation. Therefore patients with caustic ingestion
should be screened periodically for GERD and treated ag-
gressively.​8 ​In fact it may not be a bad idea to maintain
good acid control in all patients with caustic ingestion.
Miscellaneous Agents
Diverse agents such as heparin, epidermal growth
factor (EGF), and caffeic acid phenethyl ester (CAPE) have
been shown in animal studies to decrease the incidence of
stric- ture formation but studies in humans are awaited.​30,31
Ramasamy and Gumaste Corrosive Ingestion in Adults ​123
2. Gumaste VV, Dave PB. Ingestion of corrosive substances by adults. ​Am J Gas-
troenterol.​ 1992;87:1–5. 3. Moore WR. Caustic Ingestions. ​Clin Pediatr.​
1986;25:192. 4. Spiegel RJ, Sataloff RT. Caustic injuries of the Esophagus. In:
Castell DO, Richter J, eds. ​The Esophagus.​ Philadelphia: Lippincott, Williams and
Wilkins; 1999:557–564. 5. Cox AJ, Eisenbeis JF. Ingestion of Caustic hair relaxer:
Is endoscopy necessary?
Laryngoscope.​ 1997;107:897–902. 6. Zagar SA, Kochhar R, Nagar B, et al.
Ingestion of corrosive acid. ​Gastroenter-
Treatment of Strictures
Short strictures can be easily treated with endoscopic
dilatation. Long strictures that are not amenable to endo-
scopic dilatation may require surgery. Retrograde dilation
with Tuckers dilators may be attempted in severe strictures.
Intralesional injection of steroids may decrease the fre-
quency of dilation in these patients.​32 ​In the past, patients
with antral stenosis have required surgery, either pyloro-
plasty or gastroenterostomy. However, some cases may be
successfully managed with endoscopic dilatation and this
may be attempted prior to surgery.
SURGERY ​Surgery has a role to
play as an emergency measure and also later in delayed
reconstruction. In the acute phase, it is clear that patients
with evidence of perforation require im- mediate surgery.
However, some patients who do not have peritoneal signs
on admission go on to develop perforation, necrosis, and
massive bleeding later on with disastrous re- sults. Early
surgical intervention may improve the outcome in this
group of patients and certain clinical as well as en-
doscopic criteria may help in identifying this subset. Pa-
tients with shock, acidosis, and coagulation disorders and
those who have ingested large amounts of corrosives, usu-
ally tend to have severe injury on laparotomy and early
surgical intervention may prove beneficial to these
patients.​33
The finding of third degree burns on endoscopy also
merits surgical exploration according to some surgeons.​34
Zargar et al​7 ​have suggested that prompt surgical resection
may improve the mortality and morbidity in patients with
grade 3b injuries. Patients with 3a lesions may not require
emergency surgery. After recovery, surgery may be re-
quired to reconstruct the pharynx and esophagus and to
treat any gastric outlet obstruction.
REFERENCES ​1. Litovitz TL, Swartz WK, White S, et al. 2000 Annual
report of the American Association of Poison Control Centers. ​Am J Emerg Med​.
2001;19:337–395.
ology.​ 1989;97:702–707. 7. Zargar SA, Kuchhar R, Mehta S, et al. The role
of fibroptic endoscopy in the management of corrosive ingestion and modified
endoscopic classification of burns. ​Gastrointest Endosc​. 1991;37:165–169. 8. Mutaf
O, Genc A, Herek O, et al. Gastroesophageal reflux: A determinant in the
outcome of caustic esophageal burns. ​J Pediatr Surg​. 1996;31:1494–1495. 9.
Bautista A, Varela R, Villanueva A, et al. Motor function of the esophagus after
caustic burn. ​Eur J Pediatr Surg.​ 1996;6:204–207. 10. Nicosia JF, Thornton
JP, Folk FA, et al. Surgical management of corrosive gastric
 injuries. ​Ann Surg.​ 1974;180:139–143. 11. Dilwari JB, Sing S, Rao PN, et
al. Corrosive acid ingestion in man: A clinical and
endoscopic study. ​Gut.​ 1984;25:183–187. 12. Gorman RL,
Khin-Maung-Gyi MT, Klein-Schwartz W, et al. Initial symptoms as predictors of
esophageal injury in alkaline corrosive ingestion. ​Am J Emerg Med​.
1992;10:189–194. 13. Gupta SK, Croffie JM, Fitzgerald JF. Is
esophagogastroduodenoscopy necessary
in all caustic ingestions? ​J Pediatr Gastroenterol Nutr.​ 2001;32:50–53. 14.
Christensen BT. Predictions of complications following unintentional caustic
ingestion in children. ​Acta Pediatr.​ 1995;84:1177–1182. 15. Previtaria C,
Guisti F, Gugliemi M. Predictive value of visible lesions in sus-
pected caustic ingestion. ​Pediatr Emerg Care.​ 1990;6:176–178. 16. Haller
JA, Andrews HG, White JJ, et al. Pathophysiology and management of acute
corrosive burns of the esophagus: results of treatment in 285 children. ​J Pediatr Surg​.
1971;6:578–584. 17. Hawkins DB, Demeter MJ, Barnett TE. Caustic ingestion:
controversies in man-
agement. A review of 214 cases. ​Laryngoscope​. 1980;90:98–109. 18.
McAuley CE, Steel DL, Webster MW. Late sequelae of gastric acid injury. ​Am
J Surg​. 1985;149:412–415.
19. Skucas J. Contrast media. In: Gore R, Levine M, Laufer I, eds. ​Textbook of
Gastrointestinal Radiology​. Philadelphia: WB Saunders; 2000:2–14. 20. Harley EH,
Collins MD. Liquid household bleach ingestion in children. ​Laryn-
goscope.​ 1997;107:122–125. 21. Ahsan S, Haupert M. Absence of
esophageal injury in pediatric patients after hair
relaxer ingestion. ​Arch Otolaryngol Head Neck Surg.​ 1999;125:953–955. 22.
Rappert P, Preier L, Korab W, et al. Diagnostic and therapeutic management of
esophageal and caustic burns in childhood. ​Eur J Pediatr Surg​. 1993;3:202. 23. Guth
J Clin Gastroenterol, Vol 37, No. 2, 2003 ​124
AA, Pachter HL, Albanese C, et al. Combined duodenal and colonic ne- crosis and
unusual sequalae of caustic ingestion. ​J Clin Gastroenterol​. 1994;19: 303–305. 24.
Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in
children with corrosive injury of the esophagus. ​N Eng J Med​. 1990;323:637– 640.
25. Howel, Dalsey WC, Hartsell FW et al. Steroids for the treatment of corrosive
esophageal injury. A statistical analysis of past studies. ​Am J Emerg Med.​ 1992;
10:421–425. 26. Rao RB, Hoffman RS. Caustics and Batteries. In: Goldfrank LR, ed.
Goldfrank’s
Toxicologic Emergencies.​ Norwalk, CT: Appleton & Lange;
1998:1399–1428. 27. Berkovits RN, Bos CE, Wijburg FA, et al. Caustic injury of the
esophagus.
J Laryngol Otol.​ 1996;110:1041–1045. 28. De Peppo F, Zaccara A,
DallOglio L, et al. Stenting for caustic strictures.
J Pediatr Surg​. 1998;33:54–57. 29. Reddy AN, Budhraja M. Sucralfate
therapy for lye-induced esophagitis. ​Am
J Gastroenterol.​ 1988;83:71–73. 30. Bingol-Kologlu M, Tanyel FC,
Muftuoglu S, et al. The preventive effect of heparin on stricture formation after
caustic esophageal burns. ​J Pediatr Surg​. 1999;34:291–294. 31. Koltuksuz U, Mutus
HM, Kutlu R, et al. Effects of caffeic acid phenethyl ester and epidermal growth
factor on the development of caustic esophageal stricture in rats. ​J Pediatr Surg.​
2001;36:1504–1509. 32. Kochhar R, Ray JD, Shriram PV, et al. Intralesional steroids
augment the effects of endoscopic dilation in corrosive esophageal strictures.
Gastrointest Endosc​. 1999;49:509–513. 33. Wu MH, Lai WW. Surgical management
of extensive corrosive injuries of the
alimentary tract. ​Surg Gynecol Obstet.​ 1993;177:12–16. 34. Andreoni B,
Farina ML, Biffi R, et al. Esophageal perforation and caustic injury.
Dis Esophagus.​ 1997;10:95.